UBC Theses and Dissertations
The effects of systematic hypercapnia on the hindlimb perfusion pressures of acute spinal cats Accili, Eric Anthony
Normal levels of CO₂ are responsible for the maintenance of approximately 30% of sympathetic neurogenic vascular tone in intact cats. The central medullary chemoreceptors have been implicated as the major source of this CO₂ dependent neurogenic vascular tone. However, it is possible that spinal cord CO₂ sensitivity could also have mediated a portion of neurogenic vascular tone. Cats with acute and chronic spinal transections can maintain near normal levels of systemic arterial blood pressure, and show cardiovascular and sympathetic reflex changes in response to a variety of stimuli. Thus, it seemed likely that the acute spinal cat could exhibit the spinal component of CO₂ mediated sympathetic neurogenic vascular tone. Therefore the effects of systemic CO₂ increases on the perfusion pressures of vascularly isolated hindlimbs autoperfused at constant flow (as an indication of vascular resistance and sympathetic vascular tone) were studied in the acute cervical spinal cat. The contributions of the lumbar sympathetic system and the adrenal glands to perfusion pressure responses to CO₂ were evaluated. Experiments were carried out in mongrel cats with acute cervical (C2) transections. Each cat had one leg denervated by cutting and stripping the lumbar sympathetic chain from L₁-L₇. In all cats each hindlimb was vascularly isolated and perfused with blood taken from the abdominal aorta. Bilateral adrenalectomy was performed on 8 animals. CO₂ administration for 5 minutes resulted in biphasic increases in the perfusion pressures of both legs which were designated peak1 (P1) and peak2 (P2). Increasing PCO₂ from 16 to 38mm Hg, and from 16 to 62mm Hg resulted in significant P1 and P2 responses of the innervated leg. This also resulted in a significant P2 response, and an observable but insignificant P1 response, of the denervated leg. Adrenalectomy reduced P1 and P2 responses of the innervated leg, and abolished the P1 response and reduced the P2 response of the denervated leg. In non-adrenalectomized cats increasing PCO₂ also resulted in a significant increase in systemic arterial pressure (SAP) with no changes in heart rate (HR). In adrenalectomized cats increasing PCO₂ resulted in an observable but non-significant increase in SAP and a significant decrease in HR. These results suggested that: 1) The P1 response was primarily a sympathetic neurogenic response to increased CO₂. 2) The P2 response was primarily a hormonal response to CO₂ in the denervated leg, and a combination of hormonal and sympathetic neurogenic responses to CO₂ in the innervated leg. 3) The adrenal glands were mostly involved in the P2 response to CO₂, but possibly had a small role in the P1 response. 4) Other non-adrenal vasoconstrictor hormones may have played a role in the P2 response to C0₂. 5) Likely, CO₂ initially activated the sympathetic system to directly increase neurogenic tone, perhaps by stimulating sympathetic afferent or efferent neurons, or hypothetical spinal chemosensitive regions. Progressively the adrenal and possibly other unidentified vasoconstrictor hormone systems became activated, either directly by CO₂ or indirectly by CO₂ mediated sympathetic activation. These hormone systems may have also played a role in CO₂ mediated maintenance of vascular tone.
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